# Disease Tolerance in ‘Anaheim’ Pepper to PepGMV-D Strain Involves Complex Interactions Between the Movement Protein Putative Promoter Region and Unknown Host Factors

## TL;DR

This study explores how 'Anaheim' pepper plants tolerate a specific strain of a virus by examining interactions between the virus's movement protein promoter and host factors.

## Contribution

The study identifies a non-coding region's role in disease tolerance through interactions with host factors and gene silencing.

## Key findings

- Chimeric DNA-B components showed symptoms similar but not identical to wild-type infections.
- Recovered leaves had fewer transcripts and specific small interfering RNAs.
- Inefficient virus movement is linked to hyper-efficient gene silencing in 'recovered' plants.

## Abstract

Pepper golden mosaic virus (PepGMV) is a bipartite begomovirus of pepper and tomato from North America. In ‘Anaheim’ pepper plants PepGMV-Mo strain (Mo) causes systemic yellow foliar mosaic symptoms, while PepGMV-D strain (D) causes distortion of 1st–6th expanding leaves, and asymptomatic infection of subsequently developing leaves, like other known ‘recovery’ phenotypes. Infections established with DNA-A Mo and D components expressing red-shifted green fluorescent protein in place of coat protein and in situ hybridization, showed PepGMV-Mo localized to phloem and mesophyll cells, while -D was mesophyll restricted. Alignment of PepGMV-Mo and -D DNA-B components revealed three indels upstream of the BC1 gene that encodes the movement protein (MP). To determine if this non-coding region (*BC1) D-strain MP putative promoter contributed to ‘recovery’, plants were inoculated with chimeric DNA-B Mo/D components harboring reciprocally exchanged *BC1, and wild-type DNA-A Mo and D components. Symptoms were reminiscent but not identical to wild-type -Mo or -D infection, respectively, suggesting ‘recovery’ cannot be attributed solely to the *BC1. Both BC1 and D*BC1 were targeted by post-transcriptional gene silencing; however, ‘recovered’ leaves accumulated fewer transcripts and 21–24 nt vsiRNAs. Thus, inefficient in planta movement of PepGMV-D is associated with a non-pepper-adapted ‘defective’ BC1 that facilitates hyper-efficient PTGS, leading to BC1 transcript degradation that in turn limits virus spread, thereby recapitulating disease ‘tolerance’.